We will analyze by freeze-fracture intramembrane changes occurring in dystrophic as compared to normal pigment epithelial (PE) membranes during phagocytosis. PE explants will be exposed to sugar coated microspheres prior to and after the phagocytic breakdown to study whether certain intramembrane changes occur during changes in phagocytic capabilities which may reflect changes in PE membrane receptors involved in phagocytosis. We will use PE explants to study lectin receptor mobility in dystrophic and normal PE membranes during phagocytosis to test whether this mobility is altered in dystrophic PE. We will study PE cells from normal retinas in disaggregating and reaggregating cultures, first, by freeze-fracture to see how and when cell junctions between PE cells reform and how intramembrane particles on basal and apical membranes redistribute and, second, by exposing disaggregated and reaggregated PE cells to polystyrene beads to determine how PE phagocytic ability is affected before and after junctional formation. This will test whether a functional polarity of membrane receptors for phagocytosis is necessary to maintain phagocytic activity and whether it can be correlated with intramembrane changes. We will continue our objectives to localize and determine differences in carbohydrate-containing macromolecules on PE and outer segment (OS) membranes of dystrophic retinas by identifying these glycoproteins by gel electrophoresis in combination with lectin beinding techniques. These glycoproteins will be extracted and used in immunocytochemical studies to lacalize individual glycoproteins in tissue sections and on isolated PE microvilli. The long-term objectives being to localize and determine differences in carbohydrate containing macromolecules which may act as recognition molecules in phagocytosis and which may be defective dystrophic retinas. It is anticipated that this data will contribute to an understanding of the molecular basis for the breakdown in phagocytosis in inherited retinal degeneration.